The face is the mirror of the soul and facial expressions are an indispensable element of verbal and nonverbal human communication. Degenerative lesions of the facial nerve, such as tumors or traumas, lead to permanent facial nerve damage which, in contrast to many other neural lesions, cannot be hidden. Functional rehabilitation of facial nerve paresis has remained unsatisfactory despite optimal microsurgical reconstruction of the damaged nerve parts.
Unilateral damage of the nerve fibers of the facial nerve or its nucleus leads to peripheral facial paresis. This is to be distinguished from supranuclear lesions along the corticonuclear tract which lead to a so-called central facial paresis. In Western Europe and the USA, the incidence of peripheral facial pareses is approx. 20-35/100,000 inhabitants. The most frequent reasons for peripheral facial paresis are idiopathic facial paresis (two thirds of the cases, no reason can be found despite extensive diagnostics), traumatic pareses following fractures of the petrous part of the temporal bone or face injuries, inflammatory paresis accompanying chronic ear infections, and destruction of the nerve by tumors. The incidence of central facial pareses is 200/1,000,000 inhabitants, as the incidence of the most frequent cause of central facial paresis, i.e., stroke which often causes facial paresis, is 250/100,000 inhabitants. Cerebral hemorrhage, cerebral inflammation and brain tumors are less frequent causes of the central form.
Thus, facial paresis is a common disease. In most cases and depending on the cause, peripheral paresis shows non-degenerative paresis (neurapraxia according to Seddon) so that 80% of the cases show regeneration of the nerve under adequate therapy. 95% of cases with central facial paresis show regeneration. In cases of degenerative paresis (axonotmesis, neurotmesis, mixed forms according to Seddon) caused by the destruction of nerve fibers, persistent defects are observed after healing. The extent of persistent defects after healing depends on the degree of the neural lesion and the applied therapy. If only a small peripheral branch of the facial nerve is affected, mimic muscles only show very localized deficits. A complete loss of the peripheral facial nerve leads to a loss of muscle tone in the affected half of the face and the soft tissues of the face sag. Voluntary motor movement is lost, and mimic muscles can no longer be moved. The inability to close the eyelid indirectly leads to vision disorders since the eye waters and inflammation is possible. Lack of mouth movement limits speaking and eating.
In our modern society, facial expression is the essential factor of verbal and nonverbal communication. As opposed to other pareses, facial paresis cannot be hidden. Patients feel stigmatized, and often retreat from the public and develop secondary psychical disorders, e.g., depressions. The patients' quality of life is significantly curbed. Persistent defects after healing are even observed in cases of spontaneous regeneration or optimal and extensive surgical reconstruction of the nerve in cases of nerve transsection and bridging of the defect with neural transplants. Sprouting of the regenerating axons is observed at the site of the lesion even after reconstruction of nerve continuity. At the same time, Wallerian degeneration of the entire affected section of the nerve as far as the muscles is completed until only the Bungner's bands remain as Schwann cell conducting structures. The regenerating neurons with their sprouting axons grow accidentally into these bands of the individual nerve branches and are directed to the peripheral mimic muscles. Individual axons perish and do not reach the periphery, some accidentally reach their original target muscle, while others reach a completely different target muscle. Due to axonal collateral sprouting, the most frequently observed effect is simultaneous sprouting to several target muscles, such as shown in FIGS. 1A and 1B.
This leads clinically to simultaneous movement of several target muscles (a condition called synkinesis). Patients often complain about involuntary lid closure while moving the mouth, e.g., when eating. Simultaneous movement of antagonist muscles leads to the autoparalytic syndrome: muscle forces cancel each other out and no movement is observed clinically despite innervation. New research shows that not only collateral sprouting but also terminal sprouting (such as shown in FIGS. 2A and 2B) of the regenerating axons directly at the neuromuscular end-plates causes uncoordinated muscle function. This explains why the patients' quality of life is significantly limited even after surgical reconstruction of the nerve. If the lesion is so extensive that the remaining peripheral part of the facial nerve is insufficient, or if Bungner's bands are fibrosed due to failed reinnervation and muscles are atrophied due to long-term denervation of more than 3 to 5 years, the patient can no longer be offered a nerve graft.
Possible therapies include dynamic muscle grafts, free nerve-muscle transplantation, implantation of upper lid weights or static suspensions. Functional results of these secondary procedures are even less satisfactory than the above mentioned nerve grafts. These procedures may, at best, restore muscle tone, but facial expression remains very mask-like and the dynamic muscle suspensions allow reproducing only few and very mechanistic movement vectors.